The Role Of Inflammation In Heart Disease

Heart attacks are the leading cause of death in the US today. Heart disease is caused by a process called atherosclerosis in which fatty deposits called plaques gradually build up in coronary arteries, causing blockages that restrict blood flow to the heart. One out of every 2 Americans over the age of 65 has atherosclerosis, even though it is not part of the normal aging process.

The medical establishment, drug companies and the media all blame high levels of dietary cholesterol for heart attacks. However, in 1936 the pathologist Dr. Kurt Lande and biochemist Warren Sperry showed that there was no correlation between blood cholesterol levels and atherosclerosis. These findings were subsequently confirmed by a 1961 report by Indian scientists - while, two clinicians from the Beth Israel Medical Center in New York reported in 2003 that aggressive lipid-lowering by statins did not alter atherosclerosis.

The Framingham Heart Study - which examined risk factors for heart disease in over 5,000 men and women over their lifetimes - showed that 80 percent of people who go on to have coronary artery disease have the same total cholesterol values as those who don't. In other words, total cholesterol levels have absolutely nothing to do with the likelihood of developing heart disease.

So what's responsible for heart disease if not cholesterol levels?

Health experts now agree that inflammation is the most likely underlying reason for heart disease. It is also believed to contribute to the development of other diseases such as rheumatoid arthritis, Alzheimer's disease, multiple sclerosis, sepsis and others. Inflammation is a defense mechanism by which our body responds to infection or injury to limit damage, get rid of whatever is causing the problem and restore the natural balance.

Inflammation often occurs throughout our bodies as we age. As a result, many people choose to take anti-aging vitamins to help reduce inflammation and promote optimum health.

According to health experts, oxidation of LDL cholesterol and the ensuing inflammatory response triggers the formation of atherosclerotic plaques in arteries. When LDL cholesterol levels are elevated in blood, they enter the artery walls and get trapped there. This leads to their oxidation by free radicals. Oxidized LDL is very reactive and damages artery walls.

Oxidized LDL cholesterol attracts specialized white blood cells - part of the immune response system - called macrophages. They engulf oxidized LDL to stop it from causing further damage to artery walls. However, as they ingest more and more LDL, they expand and together with smooth muscle cells of the arterial cell wall, form "'foam" cells. Eventually these foam cells rupture, depositing more oxidized LDL into the artery wall - causing more macrophages to arrive at the scene, continuing the cycle and worsening the damage.

The cellular waste material left when foam cells rupture is one of the many ingredients of an atherosclerotic plaque, along with fibrin clot material. Smooth muscle cells make a collagen "'cap' to cover the site of inflammation. Calcium from blood builds up on the cap to create hardened, calcified atherosclerotic plaques.

Formation of atherosclerotic plaques is a critical first step necessary for life-threatening heart attacks to occur. Plaque formation causes arteries to become less elastic, while the lumen (through which blood flows) becomes narrower. This restricts blood and nutrient flow to tissues and raises the blood pressure needed to pump blood through the vessel, causing even more damage to the blood vessel walls. Over time, plaques grow larger, become unstable and rupture, exposing them to the contents of the blood. The entire cycle of the body's inflammatory response is repeated again and again, as the plaques grow and rupture repeatedly.

Ruptured plaques release a fatty toxin into the artery. This is seen as an injury, and the body's immune system again reacts to make a blood clot in response. Such blood clots can block blood vessels. If they form in coronary arteries, less blood and nutrients become available and the area of the heart being supplied by these arteries becomes damaged. This can cause angina, which is the pain or discomfort that occurs when not enough oxygen is available to the heart.

More seriously, clots can also cause heart attacks when blood flow is completely blocked. Plaques themselves can become so large that they block blood flow to heart muscle, killing heart muscle cells and causing heart attacks. If the clot breaks free and begins to travel through the blood, it can become stuck elsewhere in a smaller blood vessel. This is called an embolus and it can also lead to a heart attack, a stroke if it happens in the brain or a life-threatening pulmonary embolism in the lungs.

In other words, inflammation hardens arteries, leads to the formation of atherosclerotic plaques and eventually causes heart attacks. Genetics, aging, lifestyle choices, illnesses and exposure to harmful chemicals can all trigger damage to the lining of blood vessel walls, the first step towards atherosclerosis. Known risk factors that promote atherosclerosis include:

Certain bacteria (C. pneumoniae and H. pylori) and viruses (cytomegalovirus or CMV and herpes simplex or HSV) found in atherosclerotic plaques have been implicated in their formation. Other chronic diseases and infections also significantly speed up atherosclerosis.

Aging, which damages the lining of blood vessels even when cholesterol levels are normal and other risk factors are absent.

Smoking, which doubles the risk of heart attacks and may damage blood vessels by generating harmful free radical molecules.

Sign up for our exclusive offer

*BEFORE YOU TAKE ANY SUPPLEMENT, PLEASE CONSULT YOUR PHYSICIAN OR OTHER LICENSED HEALTHCARE PROFESSIONAL TO DETERMINE IF IT'S APPROPRIATE FOR YOU.*These statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat or cure any disease.